Studies showed that constitutive activation of the PI3K/AKT signaling pathway [6, 7] as well as its inhibitor, phosphatase and tensin homolog (PTEN) [8], in GCB-DLBCL plays a central role in promoting survival and chemotherapy-resistance and represents a rational therapeutic target in relapsed or refractory GCB-DLBCL. Here, AKT1 is linked to diffuse large B-cell lymphoma.